During SARS virus infection, the level of ACE2 decreased significantly, while the level of ACE was not affected (Kuba et al., 2005), which made RAAS turn to angiotensin II/AT1R axis and elevated angiotensin II level can activate NLRP3 inflammasome (Zhang et al., 2016; Zhao et al., 2018; Wang et al., 2019), thus leading to development of ARDS. This evidence concerns the gene ACE2 and acute respiratory distress syndrome.